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The immune system and the GI microbiota

The presence of intestinal bacteria plays an important role in host metabolism, the development of the intestinal epithelium, and the intestinal immune system, and it also protects the host against rapid colonisation by intestinal pathogens. To allow sufficient defence against potential pathogens but restrict the immune response to non-pathogenic resident commensal bacteria, the mucosal immune system needs to be tightly regulated.



In human inflammatory bowel diseases, e.g. in Crohn disease and ulcerative colitis, it is thought that a deregulated T-cell response to the intestinal bacterial microflora leads to chronic intestinal inflammation.








There are just theories of how dendritic immune cells (DCs) come into contact with the intestinal bacterial flora. One of them hypothesises that M cells as specialised epithelial cells can mediate the uptake of bacteria toward DCs in the intestinal lymphoid tissue (Uhlig et al, Picture source: Danone vitapole)








Obesity alters gut microbial ecology
Ruth Ley analyzed over 5.000 bacterial from the distal intestinal microbiota of genetically obese mice, wild-type siblings, and their mothers, all fed the same rich diet. Although the majority of mouse gut species are unique, the mouse and human microbiotas are similar, with Firmicutes and Bacteroidetes dominating. Microbial-community composition is inherited from mothers. However, obesity mice have a 50% reduction in the abundance of Bacteroidetes and an increase in Firmicutes. Hence, obesity affects the diversity of the gut microbiota. The intentional manipulation of community structure could be useful for regulating energy balance in obese individuals. For further reading visit also Obesity & GI microbiota.



For further information visit:
Cebra JJ. Influences of microbiota on intestinal immune system development. Am J Clin Nutr 1999;69(suppl):1046S–51S
Uhlig HH and Powrie F. Dendritic cells and the intestinal bacterial flora: a role for localized mucosal immune response. J Clin Invest 112:648-651 (2003)